Health, Obesity plus Aging Linked To Alzheimer's Markers in the Brain
Obesity Plus Aging Linked to Alzheimer’s Markers in the Brain
Summary: A new study reports high sugar and fat based diets that lead to obesity, coupled with the normal aging process, may increase the risk of Alzheimer’s disease.
Source: APS.
A new study suggests that when a high-fat, high-sugar diet that leads to obesity is paired with normal aging, it may contribute to the development of Alzheimer’s disease. In addition, researchers discovered that certain areas of the brain respond differently to risk factors associated with Alzheimer’s. The study is published in Physiological Reports.
Alzheimer’s disease, the most common form of dementia, is a progressive brain disorder that leads to loss of cognitive skills and memory and causes significant changes in behavior. Aging is a significant risk factor for Alzheimer’s. Previous studies suggest that diet-related obesity is also associated with development of the disease.
Researchers from Brock University in Ontario, Canada, looked at the effects of an obesity-inducing diet on insulin signaling (the process that tells the body how to use sugar), and markers of inflammation and cellular stress. These factors have been found to be involved in the progression of Alzheimer’s disease during the aging process in mice. One group of mice received a high-fat, high-sugar diet (“HFS”), while the control group ate a normal diet. The researchers measured the animals’ inflammation and stress levels in the hippocampus and the prefrontal cortex in the brain after 13 weeks on the assigned diets. They compared the brains of aged mice to those of a younger set of baseline mice. The hippocampus is near the center of the brain and is responsible for long-term memory. The prefrontal cortex, at the front of the brain, oversees complex cognitive, emotional and behavioral function.
Compared to the control group, the HFS group had significantly higher markers of inflammation, insulin resistance (altered insulin signaling) and cellular stress in areas of the hippocampus thought to be involved in the progression of Alzheimer’s disease. The prefrontal cortex region of the HFS group showed more signs of insulin resistance, but inflammation and cellular stress markers did not change. The “region specific differences between the prefrontal cortex and hippocampus in response to aging with a HFS diet [indicates] that the disease pathology is not uniform throughout the brain,” the researchers wrote.
Compared to the control group, the HFS group had significantly higher markers of inflammation, insulin resistance (altered insulin signaling) and cellular stress in areas of the hippocampus thought to be involved in the progression of Alzheimer’s disease. NeuroscienceNews.com image is in the public domain.
The control group’s inflammation levels were also increased after the trial when compared to the baseline readings. These results supports the theory that aging alone plays a role in the progression of Alzheimer’s disease, and obesity exacerbates the effects of aging on brain function.
“This study provides novel information in relation to the mechanistic link between obesity and the transition from adulthood to middle age and signaling cascades that may be related to [Alzheimer’s] pathology later in life,” the research team wrote. “These results add to our basic understanding of the pathways involved in the early progression of [Alzheimer’s] pathogenesis and demonstrate the negative effects of a HFS diet on both the prefrontal cortex and hippocampal regions.”
About this neuroscience research article
Funding: We acknowledge the Natural Sciences and Engineering Research Council of Canada (NSERC) for the financial support to fund this project (RGPIN‐2017‐03904 R.E.K. MacPherson) and for funding of the original in vivo trial (RGPIN 2016‐04300 S.J. Peters) as well as the Canadian Foundation for Innovation for funding of the original in vivo trial (Grant #222084 W.E. Ward). K.N. Bott was supported by an Ontario Graduate Student Scholarship. B.J. Baranowski received an Undergraduate Student Research Award from the Natural Sciences and Engineering Research Council of Canada (NSERC).
Source: Stacy Brooks – APS
Publisher: Organized by NeuroscienceNews.com.
Image Source: NeuroscienceNews.com image is in the public domain.
Original Research: Open access researchfor “Evaluation of neuropathological effects of a high‐fat high‐sucrose diet in middle‐aged male C57BL6/J mice” by Bradley J. Baranowski, Kirsten N. Bott, and Rebecca E. K. MacPherson in Physiological Reports. Published June 11 2018.
doi:10.14814/phy2.13729
Publisher: Organized by NeuroscienceNews.com.
Image Source: NeuroscienceNews.com image is in the public domain.
Original Research: Open access researchfor “Evaluation of neuropathological effects of a high‐fat high‐sucrose diet in middle‐aged male C57BL6/J mice” by Bradley J. Baranowski, Kirsten N. Bott, and Rebecca E. K. MacPherson in Physiological Reports. Published June 11 2018.
doi:10.14814/phy2.13729
Cite This NeuroscienceNews.com Article
APS”Obesity Plus Aging Linked to Alzheimer’s Markers in the Brain.” NeuroscienceNews. NeuroscienceNews, 28 June 2018.
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APS(2018, June 28). Obesity Plus Aging Linked to Alzheimer’s Markers in the Brain. NeuroscienceNews. Retrieved June 28, 2018 from http://neurosciencenews.com/obesity-aging-alzheimers-9470/
APS”Obesity Plus Aging Linked to Alzheimer’s Markers in the Brain.” http://neurosciencenews.com/obesity-aging-alzheimers-9470/ (accessed June 28, 2018).
Metabolic dysfunction related to diet‐induced obesity has recently been linked to the pathogenesis of sporadic Alzheimer’s disease (AD). However, the underlying mechanisms linking obesity and AD remain unclear. The purpose of this study was to examine early alterations in brain insulin signaling, inflammatory/stress markers, and energetic stress in a model of diet‐induced obesity during middle age. Male C57BL/6J mice were randomized to either a control diet (AGE n = 12) or high‐fat and sucrose diet (AGE‐HFS n = 12) for 13‐weeks from 20‐weeks of age. Prefrontal cortex and hippocampal samples were collected at 20‐weeks of age (BSL n = 11) and at 33‐weeks of age (AGE and AGE‐HFS). The HFS diet resulted in increased body weight (30%; P = 0.0001), increased %fat mass (28%; P = 0.0001), and decreased %lean mass (33%; P = 0.0001) compared to aged controls. In the prefrontal cortex, AGE‐HFS resulted in increased 5′ adenosine monophosphate – activated protein kinase (AMPK) phosphorylation (P = 0.045). In the hippocampus, AGE‐HFS resulted in increased extracellular signal‐regulated kinase (ERK) and c‐Jun N‐terminal kinase (JNK) phosphorylation and protein kinase B (Akt) serine473 and glycogen synthase kinase (GSK) phosphorylation (P
Metabolic dysfunction related to diet‐induced obesity has recently been linked to the pathogenesis of sporadic Alzheimer’s disease (AD). However, the underlying mechanisms linking obesity and AD remain unclear. The purpose of this study was to examine early alterations in brain insulin signaling, inflammatory/stress markers, and energetic stress in a model of diet‐induced obesity during middle age. Male C57BL/6J mice were randomized to either a control diet (AGE n = 12) or high‐fat and sucrose diet (AGE‐HFS n = 12) for 13‐weeks from 20‐weeks of age. Prefrontal cortex and hippocampal samples were collected at 20‐weeks of age (BSL n = 11) and at 33‐weeks of age (AGE and AGE‐HFS). The HFS diet resulted in increased body weight (30%; P = 0.0001), increased %fat mass (28%; P = 0.0001), and decreased %lean mass (33%; P = 0.0001) compared to aged controls. In the prefrontal cortex, AGE‐HFS resulted in increased 5′ adenosine monophosphate – activated protein kinase (AMPK) phosphorylation (P = 0.045). In the hippocampus, AGE‐HFS resulted in increased extracellular signal‐regulated kinase (ERK) and c‐Jun N‐terminal kinase (JNK) phosphorylation and protein kinase B (Akt) serine473 and glycogen synthase kinase (GSK) phosphorylation (P
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